article · Environmental Science and Pollution Research
Silver nanoparticles are widely utilised in medicine and the food industry, yet concerns persist regarding their safety for human health and the environment. An experimental investigation in male Sprague Dawley rats evaluated the liver toxicity caused by daily intraperitoneal administration of silver nanoparticles at three doses over 15 and 30 days. Exposure caused decreased body weight, haematological alterations, and significant oxidative and nitrosative stress in the liver, marked by depleted glutathione levels. The treatment also increased serum markers of liver injury and induced dose- and duration-dependent structural damage, primarily cholangiopathy. Mechanistic assessments revealed that the nanoparticles trigger liver cell death by upregulating pro-apoptotic markers such as caspase-3 and BAX while downregulating the anti-apoptotic marker Bcl-2. Furthermore, activation of TGF-beta 1, alpha-SMA, and iNOS pathways promoted liver fibrosis and persistent inflammation.
Silver nanoparticles are increasingly incorporated into medical treatments and commercial food products. Understanding their toxic effects on major organs such as the liver helps establish safe exposure limits. Identifying the biological mechanisms that cause cell death and fibrosis provides crucial data needed to guide chemical safety regulations and consumer protection policies.
This is early-stage toxicological research in an animal model. The abstract does not indicate a commercial application pathway, but the mechanistic findings could inform product safety assessments, regulatory evaluations, and risk mitigation strategies for chemical manufacturers, pharmaceutical developers, and food industry stakeholders who utilise silver nanoparticles.
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Despite the extraordinary use of silver nanoparticles (AgNPs) in medicinal purposes and the food industry, there is rising worry about potential hazards to human health and the environment. The existing study aims to assess the hepatotoxic effects of different dosages of AgNPs by evaluating hematobiochemical parameters, oxidative stress, liver morphological alterations, immunohistochemical staining, and gene expression to clarify the mechanism of AgNPs' hepatic toxic potential. Forty male Sprague Dawley rats were randomly assigned into control and three AgNPs intraperitoneally treated groups 0.25, 0.5, and 1 mg/kg b.w. daily for 15 and 30 days. AgNP exposure reduced body weight, caused haematological abnormalities, and enhanced hepatic oxidative and nitrosative stress with depletion of the hepatic GSH level. Serum hepatic injury biomarkers with pathological hepatic lesions where cholangiopathy emerges as the main hepatic alteration in a dosage- and duration-dependent manner were also elevated. Furthermore, immunohistochemical labelling of apoptotic markers demonstrated that Bcl-2 was significantly downregulated while caspase-3 was significantly upregulated. In conclusion, the hepatotoxic impact of AgNPs may be regulated by two mechanisms, implying the apoptotic/antiapoptotic pathway via raising BAX and inhibiting Bcl-2 expression levels in a dose-dependent manner. The TGF-β1 and α-SMA pathway which triggered fibrosis with incorporation of iNOS which consequently activates the inflammatory process were also elevated. To our knowledge, there has been no prior report on the experimental administration of AgNPs in three different dosages for short and long durations in rats with the assessment of Bcl-2, BAX, iNOS, TGF-β1, and α-SMA gene expressions.
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DOI: 10.1007/s11356-022-21388-3
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